Ask about this productRelated genes to: C19ORF24 Blocking Peptide
- Gene:
- C19orf24 NIH gene
- Name:
- chromosome 19 open reading frame 24
- Previous symbol:
- -
- Synonyms:
- FLJ20640
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-16
- Date modifiied:
- 2016-09-30
Related products to: C19ORF24 Blocking Peptide
Related articles to: C19ORF24 Blocking Peptide
- The role of RNA N6-methyladenosine (m6A) modifications in modulating the immune microenvironment during ischemic stroke (IS) pathogenesis remains poorly characterized. This investigation systematically explores m6A-mediated immune regulation in IS and identifies critical immune-related biomarkers. Transcriptomic profiles from 108 IS samples were analyzed to discern m6A regulatory patterns. Single-sample gene set enrichment analysis (ssGSEA) and gene set variation analysis (GSVA) quantified immune cell infiltration and pathway activity across IS subtypes and controls. Weighted gene co-expression network analysis (WGCNA) identified m6A-associated gene modules. Two complementary machine learning approaches were applied to identify the key immune-related genes implicated in IS pathogenesis. The robustness of these findings was subsequently confirmed through a comprehensive meta-analysis integrating six independent datasets. Eight dysregulated m6A regulators distinguished IS from controls. Unsupervised clustering delineated two distinct m6A modification patterns (Clusters A/B) with divergent immune landscapes: Cluster B exhibited heightened infiltration of natural killer cells, eosinophils, and activated CD4 T cells, coupled with IL6/JAK/STAT3 pathway activation, whereas Cluster A demonstrated enrichment of immature dendritic cells and monocytes, alongside oxidative phosphorylation signaling. WGCNA identified a conserved immune-related module (black module, = 0.68 with Cluster B) containing 322 co-expressed genes. Cross-validation by machine learning nominated five candidate biomarkers (, , , , C19orf24) showing consistent expression trends in internal validation cohorts (Control vs. IS and Cluster A vs. B). External validation via meta-analysis confirmed as a protective factor against IS susceptibility (odds ratio [OR] = 0.74, 95% confidence interval [CI]: 0.57–0.97), while (OR = 1.46, 95% CI: 1.01–2.10) and (OR = 1.57, 95% CI: 1.12–2.22) were significantly associated with increased IS susceptibility, establishing their roles as risk genes. Subsequent RT-qPCR analysis in clinical samples further validated the results of the aforementioned external validation. Moreover, ROC analysis revealed an AUC of 0.88 (95% CI: 0.82–0.94) for , 0.82 (95% CI: 0.74–0.89) for , and 0.90 (95% CI: 0.84–0.96) for . This study establishes m6A epitranscriptomic remodeling as a pivotal orchestrator of immune microenvironment heterogeneity in IS. The identification of , , and as promising biomarkers not only enhances the potential for precise diagnosis but also provides actionable targets for immunomodulatory therapy in IS. - Source: PubMed
Publication date: 2025/08/28
Zheng Peng-FeiHuang Cheng-ChengWang Chang-LuZhou TingPan Hong-WeiHe JinHong Xiu-QinHuang Li-ZhongRong Jing-JingShi Xiang-Jiang - Wilms tumor (WT) and Rhabdoid tumor (RT) are pediatric renal tumors and their differentiation is based on histopathological and molecular analysis. The present study aimed to introduce the panels of mRNAs and microRNAs involved in the pathogenesis of these cancers using deep learning algorithms. Filter, graph, and association rule mining algorithms were applied to the mRNAs/microRNAs data. Candidate miRNAs and mRNAs with high accuracy (AUC: 97%/93% and 94%/97%, respectively) could differentiate the WT and RT classes in training and test data. Let-7a-2 and C19orf24 were identified in the WT, while miR-199b and RP1-3E10.2 were detected in the RT by analysis of Association Rule Mining. The application of the machine learning methods could identify mRNA/miRNA patterns to discriminate WT from RT. The identified miRNAs/mRNAs panels could offer novel insights into the underlying molecular mechanisms that are responsible for the initiation and development of these cancers. They may provide further insight into the pathogenesis, prognosis, diagnosis, and molecular-targeted therapy in pediatric renal tumors. - Source: PubMed
Publication date: 2023/08/07
Hosseiniyan Khatibi Seyed MahdiRahbar Saadat YaldaHejazian Seyyedeh MinaSharifi SiminArdalan MohammadrezaTeshnehlab MohammadZununi Vahed SepidehPirmoradi Saeed - Early identification of metastatic or recurrent colorectal cancer (CRC) patients who will be sensitive to FOLFOX (5-FU, leucovorin and oxaliplatin) therapy is very important. We performed microarray meta-analysis to identify differentially expressed genes (DEGs) between FOLFOX responders and nonresponders in metastatic or recurrent CRC patients, and found that the expression levels of WASHC4, HELZ, ERN1, RPS6KB1, and APPBP2 were downregulated, while the expression levels of IRF7, EML3, LYPLA2, DRAP1, RNH1, PKP3, TSPAN17, LSS, MLKL, PPP1R7, GCDH, C19ORF24, and CCDC124 were upregulated in FOLFOX responders compared with nonresponders. Subsequent functional annotation showed that DEGs were significantly enriched in autophagy, ErbB signaling pathway, mitophagy, endocytosis, FoxO signaling pathway, apoptosis, and antifolate resistance pathways. Based on those candidate genes, several machine learning algorithms were applied to the training set, then performances of models were assessed via the cross validation method. Candidate models with the best tuning parameters were applied to the test set and the final model showed satisfactory performance. In addition, we also reported that MLKL and CCDC124 gene expression were independent prognostic factors for metastatic CRC patients undergoing FOLFOX therapy. - Source: PubMed
Publication date: 2020/01/01
Lu WeiFu DongliangKong XiangxingHuang ZhihengHwang MaxwellZhu YingshuangChen LiuboJiang KaiLi XinlinWu YihuaLi JunYuan YingDing Kefeng - The Peutz-Jeghers Syndrome (PJS) is an autosomal dominant polyposis disorder with increased risk of multiple cancers. STK11/LKB1 (hereafter named STK11) germline mutations account for the large majority of PJS cases whereas large deletions account for about 30% of the cases. We report here the first thorough molecular characterization of 15 large deletions identified in a cohort of 51 clinically well-characterized PJS patients. The deletions were identified by MLPA analysis and characterized by custom CGH-array and quantitative PCR to define their boundaries. The deletions, ranging from 2.9 to 180 kb, removed one or more loci contiguous to the STK11 gene in six patients, while partial STK11 gene deletions were present in the remaining nine cases. By means of DNA sequencing, we were able to precisely characterize the breakpoints in each case. Of the 30 breakpoints, 16 were located in Alu elements, revealing non-allelic homologous recombination (NAHR) as the putative mechanism for the deletions of the STK11 gene, which lays in a region with high Alu density. In the remaining cases, other mechanisms could be hypothesized, such as microhomology-mediated end-joining (MMEJ) or non-homologous end-joining (NHEJ). In conclusion we here demonstrated the non-random occurrence of large deletions associated with PJS. All our patients had a classical PJS phenotype, which shows that haploinsufficiency for SBNO2, C19orf26, ATP5D, MIDN, C19orf23, CIRBP, C19orf24,and EFNA2, does not apparently affect their clinical phenotype. - Source: PubMed
Publication date: 2010/07/11
Resta NicolettaGiorda RobertoBagnulo RosannaBeri SilvanaDella Mina ErikaStella AlessandroPiglionica MarilidiaSusca Francesco ClaudioGuanti GinevraZuffardi OrsettaCiccone Roberto - Secreted proteins play important roles in many crucial biological processes, and can be new agents or targets for drug therapies. Here, we report on the isolation and characterization of a novel human non-classical secreted protein which is encoded by the hypothetical gene C19orf24 (chromosome 19 open reading frame 24). It has no signal peptide, but can still secrete extracellularly despite the presence of the inhibitor brefeldin A (BFA), proving its non-classical secreted protein status. Via subcellular localization using C19orf24 in vivo and transfected pEYFP-Golgi plasmid in Hela cells, C19orf24 was shown not to co-localize in the Golgi apparatus, which suggested that it secretes via a new and unknown pathway. Deglycosylation analysis with PNGase F verified that it has no N-glycosylation modification sites. Via the reverse transcription-PCR method, it was found to be expressed only in the human liver, and preferentially in normal tissue. In addition, C19orf24 was shown to be a recently evolved gene, found only in Homo sapiens and Pan troglodytes. By calculating its synonymous and non-synonymous substitution rate (d (S)/d (N)), we found that it experienced a purifying selection, which suggests that C19orf24 may have a special, irreplaceable biological function in the human organism. - Source: PubMed
Wang Xin-RongZhou Yu-BoLiu FengWang Ke-ShengShen YanLiu Jian-HuaHan Ze-Guang